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anti-Human Oncostatin M Antibodies:
anti-Mouse (Murine) Oncostatin M Antibodies:
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Human Polyclonal Oncostatin M Primary Antibody for CyTOF, FACS - ABIN4899954
Ohsaka, Hirota-Komatsu, Shibata, Ezaki, Shinohara, Yoshida: Specific association of increased vascular endothelial growth factor expression and its receptors with macrophage differentiation of HL-60 leukemia cells. in Biochemical and biophysical research communications 2008
Show all 2 Pubmed References
Human Polyclonal Oncostatin M Primary Antibody for IHC (p), WB - ABIN3043117
Zhu, Che, Liao, Wang, Wang, Chen, Wang, Dai, Wan: Oncostatin M activates STAT3 to promote endometrial cancer invasion and angiogenesis. in Oncology reports 2015
Human Monoclonal Oncostatin M Primary Antibody for IHC, IHC (p) - ABIN4341424
Kang, Kim, Jang, Park, Lee, Kim: 22q11-q13 as a hot spot for prediction of disease-free survival in bile duct cancer: integrative analysis of copy number variations. in Cancer genetics 2014
Human Polyclonal Oncostatin M Primary Antibody for ELISA (Detection), FACS - ABIN4899952
Hurst, McLoughlin, Monslow, Owens, Morgan, Fuller, Topley, Jones: Secretion of oncostatin M by infiltrating neutrophils: regulation of IL-6 and chemokine expression in human mesothelial cells. in Journal of immunology (Baltimore, Md. : 1950) 2002
H3N2 influenza virus infection enhances oncostatin M expression in human nasal epithelium.
our findings suggest that OSM plays a crucial role in the early steps of metastatic breast cancer progression, resulting in increased circulating tumor cell (CTC) and lung metastases as well as reduced survival. Therefore, early therapeutic inhibition of OSM in patients with breast cancer may prevent breast cancer metastasis.
data reveal that individual amino acids within the AB loop of OSM determine species-specific activities. These mutations might reflect a key step in the evolutionary process of this cytokine, in which receptor promiscuity gives way to ligand-receptor specialization.
Because most of the key amino acid residues identified here are conserved between LIF and OSM, we concluded that comparatively minor differences in a few amino acid residues within binding site III account for the differential biological effects of OSM and LIF
The mechanism of prostaglandin E2-induced transcriptional up-regulation of Oncostatin-M by CREB and Sp1 has been described.
OSM [oncostatin M]might be involved in the invasiveness of extravillous trophoblasts under hypoxia conditions via increasing MMP-2 and MMP-9 enzymatic activities through STAT3 signaling. Increased MMP-9 activity by OSM seems to be more important in primary trophoblasts.
IL6 family cytokine oncostatin-M (OSM) induced a switch to the EMT phenotype and protected cells from targeted drug-induced apoptosis in OSM receptors (OSMRs)/JAK1/STAT3-dependent manner
Oncostatin M induces RIG-I and MDA5 expression and enhances the double-stranded RNA response in fibroblasts.
The IL-6-type cytokine oncostatin M (OSM) indeed induces cellular properties associated with tumorigenesis and disease progression in non-transformed human prostate epithelial cells, including morphological changes, epithelial-to-mesenchymal transition (EMT), enhanced migration and pro-invasive growth patterns.
downregulation of miR-20a-5p is caused by promoter hypermethylation. MiR-20a-5p could also suppress the production of IL-17 by targeting OSM and CCL1 production in CD4(+) T cells in patients with active VKH.
our findings suggested that OSM suppresses SLUG expression and tumor metastasis of lung adenocarcinoma cells through inducing the inhibitory effect of the STAT1-dependent pathway and suppressing the activating effect of STAT3-dependent signaling
Genistein (a specific Tyr phosphorylation inhibitor) leads to the interaction of CHOP (C/EBP Homologous Protein) with C/EBP-beta, thus negatively regulating it. Knockdown of C/EBP-beta also leads to inhibition of PMA-mediated OSM induction.
Data provide evidence that OSM regulates an epithelial-mesenchymal transition and cancer stem cell plasticity program that promotes tumorigenic properties in pancreatic cells.
OSM-induced plasticity was Signal Transducer and Activator of Transcription 3 (STAT3)-dependent, and also required a novel intersection with transforming growth factor-beta (TGF-beta)/SMAD signaling. Removal of OSM or inhibition of STAT3 or SMAD3 resulted in a marked reversion to a non-invasive, epithelial phenotype.
Neutrophils are a major source of OSM-producing cells in patients with chronic rhinosinusitis and severe asthma.
OSM and OSMR are highly expressed in inflammatory bowel disease intestinal mucosa compared to control mucosa. OSM promotes inflammatory behavior in human intestinal stroma.
Study showed that in atrial fibrillation (AF) with thrombus, the atrial tissue infiltration of M1 macrophages increased significantly; the OSM expression was also found to increase simultaneously; downstream tissue factor (TF) increased and tissue factor pathway inhibitors (TFPI)decreased, leading to an imbalance between TF and TFPI eventually. OSM might be related to thrombosis in patients with AF mediated by TF and TFPI
a novel STAT3/SMAD3-signaling axis is required for OSM-mediated senescence.
This result demonstrates that HPV16 oncoproteins upregulate oncostatin M and play an important role to promote oral squamous cell carcinoma development
The identification of the OSM inflammatory pathway as an important mediator of epithelial mesenchymal transition in triple-negative breast cancer (TNBC) may provide a novel potential opportunity to improve therapeutic strategies.
OSM, part of the interleukin 6 cytokine family, is a HIF-1alpha target gene, which directly inhibits the TGF-beta1 mediated activation of cardiac fibroblasts through extracellular signal-regulated kinase 1/2-dependent phosphorylation of the SMAD linker region.
distinct roles for OSM and IL-6 in M2 macrophage polarization, are reported.
Oncostatin M is a secreted niche factor responsible for quiescence induction
data revealed that OSM alleviated postinfarction cardiac remodeling and dysfunction by enhancing cardiomyocyte autophagy. OSM holds promise as a therapeutic target in treating HF after MI through Obeta receptor by inhibiting Mst1 phosphorylation.
TRAF5 is crucially involved in OSM-mediated lung inflammation probably by inducing lung stromal/fibroblast cell activation.
OSM mitigated the proliferation of Th17 cells and decreased the expression of IL-17 and IL-21; it promoted the activation of suppressor of cytokine signaling 3 (SOCS3), STAT3, and STAT5; observations suggest that OSM can inhibit Th17 differentiation by reciprocally controlling SOCS3, STAT3, and STAT5
In an animal model of anti-TNF-resistant intestinal inflammation, genetic deletion or pharmacological blockade of OSM significantly attenuates colitis.
these results support the proinflammatory role of OSM when it is overexpressed in the skin. However, OSM expression was not required in the murine model of psoriasis induced by topical application of imiquimod, as demonstrated by the inflammatory phenotype of OSM-deficient mice or wild-type mice treated with anti-OSM antibodies.
OSM (mOSM) signals mainly via an OSM receptor (OSMR)-gp130 heterodimer and binds with only very low affinity to mLIFR.
Loss of Oncostatin M Signaling in Adipocytes Induces Insulin Resistance and Adipose Tissue Inflammation in Vivo.
mechanism of OSM-induced cardiomyocyte dedifferentiation is associated with B-Raf/Mek/Erk signaling pathway through the OSM receptor Obeta
Oncostatin M and interleukin-31: Cytokines, receptors, signal transduction and physiology.
OSM plays multiple critical roles in the maintenance and development of the hematopoietic microenvironment in the bone marrow at a steady state as well as after injury.
OSM treatment preserved cardiac function, inhibited apoptosis and fibrosis, and stimulated angiogenesis via upregulating VEGF and bFGF in infarct border zone of ischemic myocardium, indicating that OSM could be a novel therapeutic target for MI.
The mechanism of Oncostatin M on cardiac ischemia/reperfusion injury is partly mediated by the Notch3/Akt pathway.
OSM-induced osteogenesis and upregulation of osteogenic gene products require activity of PKCdelta.
The Notch signaling pathway was found to be one of the signaling pathways that inhibit OSM-induced MC3T3-E1 cell proliferation and differentiation.
administration of Fstl1 induced airway remodeling and increased OSM, whereas administration of an anti-OSM Ab blocked the effect of Fstl1 on inducing airway remodeling, eosinophilic airway inflammation
These findings provide the first evidence that OSM receptor is regulated during follicle atresia, ovulation and luteolysis, and that OSM from other cells may mediate granulosa and luteal cell function, regulating the expression of genes involved in cell's viability.
Protein kinase R plays a pivotal role in oncostatin M and interleukin-1 signalling in bovine articular cartilage chondrocytes.
Oncostatin M is a member of a cytokine family that includes leukemia-inhibitory factor, granulocyte colony-stimulating factor, and interleukin 6. This gene encodes a growth regulator which inhibits the proliferation of a number of tumor cell lines. It regulates cytokine production, including IL-6, G-CSF and GM-CSF from endothelial cells.